Health Boards
Mon-26-11-2012, 12:17 PM
Research has shown that antibodies designed to block two proteins involved in inflammation, can reduce features of Alzheimer’s in mice. This study uses similar antibodies to ones approved for treatment of psoriasis.
There is increasing evidence that inflammation in the brain can play a role in Alzheimer’s disease. Specialist immune cells in the brain called microglia are thought to be involved in the inflammatory response in the brain that may contribute to the disease.
To study this further, the scientists from Universities in Germany and Switzerland studied mice bred to develop features of Alzheimer’s. The team discovered that the mice had high levels of two messengers called IL-12 and IL-23 in the brain. Both are made up of protein building blocks, and a protein called p40 is a common component of both. The researchers stopped the p40 protein from being produced in the mice and observed a marked decrease in brain levels of the hallmark Alzheimer’s protein amyloid.
The team then used antibodies designed to stick to p40 and stop it from working. The antibodies were given to the mice for 60 days and the team saw both a reduction in amyloid levels and an improvement in the cognitive problems normally seen in these mice.
When the researchers looked for p40 in cerebrospinal fluid of people, they found higher p40 levels in people with Alzheimer’s compared to those without the disease.
Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“There is increasing evidence that inflammation is a key player in Alzheimer’s and it is an exciting area for researchers working to defeat this devastating disease. This promising research adds further support for the role of the immune system in Alzheimer’s, linking two inflammatory proteins to the disease in mice. Early studies like these are crucial to help highlight new targets for drug development, but we need to be careful not to assume that what is true for mice is true for men. Before any new Alzheimer’s drug can reach patients, first it must be rigorously tested in clinical trials.
Source: NO LINKS ALLOWED
There is increasing evidence that inflammation in the brain can play a role in Alzheimer’s disease. Specialist immune cells in the brain called microglia are thought to be involved in the inflammatory response in the brain that may contribute to the disease.
To study this further, the scientists from Universities in Germany and Switzerland studied mice bred to develop features of Alzheimer’s. The team discovered that the mice had high levels of two messengers called IL-12 and IL-23 in the brain. Both are made up of protein building blocks, and a protein called p40 is a common component of both. The researchers stopped the p40 protein from being produced in the mice and observed a marked decrease in brain levels of the hallmark Alzheimer’s protein amyloid.
The team then used antibodies designed to stick to p40 and stop it from working. The antibodies were given to the mice for 60 days and the team saw both a reduction in amyloid levels and an improvement in the cognitive problems normally seen in these mice.
When the researchers looked for p40 in cerebrospinal fluid of people, they found higher p40 levels in people with Alzheimer’s compared to those without the disease.
Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“There is increasing evidence that inflammation is a key player in Alzheimer’s and it is an exciting area for researchers working to defeat this devastating disease. This promising research adds further support for the role of the immune system in Alzheimer’s, linking two inflammatory proteins to the disease in mice. Early studies like these are crucial to help highlight new targets for drug development, but we need to be careful not to assume that what is true for mice is true for men. Before any new Alzheimer’s drug can reach patients, first it must be rigorously tested in clinical trials.
Source: NO LINKS ALLOWED